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Reduction by prostaglandin E 1 or prostaglandin E 0 of myocardial infarct size in the rabbit by activation of ATP‐sensitive potassium channels
Author(s) -
Hide Emma J.,
Ney Peter,
Piper Julie,
Thiemermann Christoph,
Vane John R.
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb15092.x
Subject(s) - glibenclamide , prostaglandin , medicine , prostaglandin e , potassium channel , myocardial infarction , prostaglandin e1 , anesthesia , ischemia , cardiology , endocrinology , chemistry , diabetes mellitus
1 This study examined whether pretreatment of rabbits with infusions of prostaglandin E l (PGE 1 ) or prostaglandin E 0 (PGE 0 ) (which were terminated prior to the onset of ischaemia) reduce myocardial infarct size arising from coronary artery occlusion (60 min) and reperfusion (120 min). In addition, we investigated whether the observed cardioprotective effects of these two prostaglandins were due to the activation of ATP‐sensitive potassium (K ATP ) channels. 2 In the anaesthetized rabbit, infarct size (expressed as a percentage of the area at risk) after 60 min of coronary artery occlusion followed by 2 h of reperfusion was 59±4% (n= 10). PGE 1 or PGE 0 treatment (1.0 μg kg −1 min −1 ), administered as 1 h pretreatments (0.05 ml min −1 , i.v.), significantly reduced infarct size to 44±6% (n = 6) or 42±1% (n = 6), respectively. PGE 1 or PGE 0 pretreatment resulted in a significant reduction in mean arterial blood pressure, which returned to baseline within 15 min of discontinuation of the infusion (i.e. prior to LAL ligation). 3 The reduction in infarct size afforded by PGE 1 was abolished by pretreatment of rabbits with the K ATP channel blockers, glibenclamide (60±4%; n = 8) or 5‐hydroxydecanoate (58±6%; n = 6). Similarly, glibenclamide also largely attenuated the reduction in infarct size afforded by PGE 0 (52±3%; n = 8). 4 We propose that a 1 h pretreatment of PGE 1 or PGE 0 reduces infarct size by activating protein kinase C resulting in the opening of K ATP channels.